Functional analysis of a set of genes related to the molecular targeted therapy resistance in glioblastoma and the development of novel therapeutic strategies
Project/Area Number |
23390343
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Research Category |
Grant-in-Aid for Scientific Research (B)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Cerebral neurosurgery
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Research Institution | The University of Tokyo |
Principal Investigator |
MUKASA Akitake 東京大学, 医学部附属病院, 講師 (90463869)
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Co-Investigator(Kenkyū-buntansha) |
SAITO Kuniaki 杏林大学, 医学部, 助教 (50446564)
TANAKA Minoru 東京大学, 医学部付属病院, 助教 (50332581)
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Research Collaborator |
OHTANI Rhyohei
OMATA Mayu
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Project Period (FY) |
2011-04-01 – 2015-03-31
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Project Status |
Completed (Fiscal Year 2014)
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Budget Amount *help |
¥18,850,000 (Direct Cost: ¥14,500,000、Indirect Cost: ¥4,350,000)
Fiscal Year 2013: ¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2012: ¥6,240,000 (Direct Cost: ¥4,800,000、Indirect Cost: ¥1,440,000)
Fiscal Year 2011: ¥7,540,000 (Direct Cost: ¥5,800,000、Indirect Cost: ¥1,740,000)
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Keywords | 膠芽腫 / 分子標的治療 / 治療耐性 / EGFR / 腫瘍幹細胞 / 脳腫瘍幹細胞 / 分子標的療法 |
Outline of Final Research Achievements |
Molecular targeted therapy against epidermal growth factor receptor (EGFR)had been tested for malignant gliomas (glioblastomas), however, the efficacy was limited since the tumors rapidly became resistant to the targeted therapy. In this study, we analyzed the function of a set of resistance-related genes that we identified in the previous study and called “SDeltaE” (the substitute for Delta EGFR expression). Some of candidate SDletaE genes were revealed to be upregulated in glioma-initiating cells. Inhibition of these SDeltaE led to suppression of tumor cell growth and invasion. Hence, these genes were expected be the novel targets in malignant gliomas.
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Report
(4 results)
Research Products
(28 results)
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[Journal Article] H3F3A K27M mutations in thalamic gliomas from young adult patients2014
Author(s)
Aihara K, Mukasa A, Gotoh K, Saito K, Nagae G, Tsuji S, Tatsuno K, Yamamoto S, Takayanagi S, Narita Y, Shibui S, Aburatani H, Saito N
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Journal Title
Neuro Oncol
Volume: 16
Issue: 1
Pages: 140-146
DOI
Related Report
Peer Reviewed / Open Access / Acknowledgement Compliant
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[Journal Article] Mutational analysis reveals the origin and therapy-driven evolution of recurrent glioma2014
Author(s)
Johnson BE, Mazor T, Hong C, Barnes M, Aihara K, McLean CY, Fouse SD, Yamamoto S, Ueda H, Tatsuno K, Asthana, Jalbert, Nelson, Bollen, Gustafson, Charron, Weiss, Smirnov, Song, Olshen, Cha, Zhao, Moore, Mungall, Jones SJ, Hirst M, Marra MA, Saito N, Aburatani H, Mukasa A, Berger S, Chang SM, Taylor BS, Costello JF
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Journal Title
Science
Volume: 343
Issue: 6167
Pages: 189-193
DOI
Related Report
Peer Reviewed / Open Access
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[Journal Article] PCDH10 is required for the tumorigenicity of glioblastoma cells2014
Author(s)
Kanae Echizen, Mitsutoshi Nakada , Tomoatsu Hayashi, Hemragul Sabit, Takuya Furuta, Miyuki Nakai, Ryo Koyama-Nasu, Yukiko Nishimura, Kenzui Taniue, Yasuyuki Morishita, Shinji Hirano, Kenta Terai, Tomoki Todo, Yasushi Ino, Akitake Mukasa, Shunsaku Takayanagi, Ryohei Ohtani, Nobuhito Saito, Tetsu Akiyama
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Journal Title
Biochem. Biophys. Res. Commun.
Volume: 444
Issue: 1
Pages: 13-18
DOI
Related Report
Peer Reviewed / Open Access
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[Presentation] Tumor suppressive role of DACH1 in glioblastoma stem-like cell2013
Author(s)
5.Akitake Mukasa, Akira Watanabe, Hideki Ogiwara, Nobuhito Saito, Hiroyuki Aburatani
Organizer
The 4th Quadrennial Meeting of the World Federation of Neuro-Oncology (WFNO)/ the 18th Annual Society for Neuro-Oncology (SNO) Meeting
Place of Presentation
San Francisco (USA)
Year and Date
2013-11-22 – 2013-11-25
Related Report
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